钙激活氯通道与哮喘黏液过度分泌及气道炎症的关系  

Relationship between calcium-activated chloride channels and mucus overproduction,allergic airway inflammation in asthma

作　　者：姜轶飞[1,2] 沈华浩[1] 

机构地区：[1]浙江大学医学院附属第二医院呼吸科,浙江杭州310009 [2]浙江省嘉兴市第二医院呼吸科,浙江嘉兴314000

出　　处：《中国病理生理杂志》2010年第9期1863-1866,共4页Chinese Journal of Pathophysiology

摘　　要：哮喘的一个重要特征是杯状细胞增生和黏液过度分泌，大量黏液难以清除引起小气道阻塞并导致气道高反应性，急性哮喘死亡患者尸检显示大小气道均有杯状细胞增生和黏液过度分泌，这种黏液过度分泌导致的气道阻塞是重症哮喘主要死因之一，有研究证实黏液过度分泌是第1秒用力呼气容积（FEV1）下降加速的独立危险因素。Calcium -activated chloride channels play important roles in the pathological processes in asthma with mucus overproduction and a series of airway inflammation. The function of calcium - activated chloride channels de- pends on their structure and characterization. The members of chloride channels, calcium activated （CLCA） family of pro- teins and in particular murine mCLCA3 （ alias Gob - 5 ） are possible initial factors of mucus overproduction in asthma. Regulation of mCLCA3 is relevant with cytokines secreted by Th2 cells. Over - expression of Gob - 5 and hCLCA1 increase the translation of MUC5AC gene, which upregulates the secretion of goblet cells. Further sttrdy on the function and structure of calcium activated chloride channels may provide new evidence for understanding the pathogenesis of asthma.

关 键 词：钙激活氯通道 小鼠 哮喘 

分 类 号：R562.25[医药卫生—呼吸系统]